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Knockdown of death receptor 5 antisense long noncoding RNA and cisplatin treatment modulate similar macromolecular and metabolic changes in HeLa cells. 敲低死亡受体5反义长链非编码RNA和顺铂治疗可调节HeLa细胞类似的大分子和代谢变化。
Pub Date : 2022-01-01 DOI: 10.55730/1300-0152.2634
Dilek Cansu Gürer, İpek Erdoğan Vatansever, Çağatay Ceylan, Bünyamin Akgül

Background/aim: Despite great progress in complex gene regulatory mechanisms in the dynamic tumor microenvironment, the potential contribution of long noncoding RNAs (lncRNAs) to cancer cell metabolism is poorly understood. Death receptor 5 antisense (DR5-AS) is a cisplatin inducible lncRNA whose knockdown modulates cell morphology. However, its effect on cell metabolism is unknown. The aim of this study is to examine metabolic changes modulated by cisplatin and DR5-AS lncRNA in HeLa cells.

Materials and methods: We used cisplatin as a universal cancer therapeutic drug to modulate metabolic changes in HeLa cervix cancer cells. We then examined the extent of metabolic changes by Fourier transform infrared spectroscopy (FTIR). We also performed transcriptomics analyses by generating new RNA-seq data with total RNAs isolated from cisplatin-treated HeLa cells. Then, we compared cisplatin-mediated transcriptomics and macromolecular changes with those mediated by DR5-AS knockdown.

Results: Cisplatin treatment caused changes in the unsaturated fatty acid and lipid-to-protein ratios and the glycogen content. These observations in altered cellular metabolism were supported by transcriptomics analyses. FTIR spectroscopy analyses have revealed that DR5-AS knockdown causes a 20.9% elevation in the lipid/protein ratio and a 76.6% decrease in lipid peroxidation. Furthermore, we detected a 3.42% increase in the chain length of the aliphatic lipids, a higher content of RNA, and a lower amount of glycogen indicating relatively lower metabolic activity in the DR5-AS knockdown HeLa cells. Interestingly, we observed a similar gene expression pattern under cisplatin treatment and DR5-AS knockdown HeLa cells.

Conclusion: These results suggest that DR5-AS lncRNA appears to account for a fraction of cisplatin-mediated macromolecular and metabolic changes in HeLa cervix cancer cells.

背景/目的:尽管在动态肿瘤微环境中复杂基因调控机制的研究取得了很大进展,但长链非编码rna (lncRNAs)对癌细胞代谢的潜在贡献尚不清楚。死亡受体5反义(DR5-AS)是一种顺铂诱导的lncRNA,其敲低可调节细胞形态。然而,其对细胞代谢的影响尚不清楚。本研究的目的是研究顺铂和DR5-AS lncRNA在HeLa细胞中调节的代谢变化。材料和方法:我们将顺铂作为一种通用的癌症治疗药物来调节HeLa宫颈癌细胞的代谢变化。然后我们用傅里叶变换红外光谱(FTIR)检测了代谢变化的程度。我们还通过从顺铂处理的HeLa细胞中分离的总rna产生新的RNA-seq数据进行转录组学分析。然后,我们比较了顺铂介导的转录组学和大分子变化与DR5-AS敲低介导的转录组学和大分子变化。结果:顺铂治疗引起不饱和脂肪酸、脂蛋白比和糖原含量的改变。这些在细胞代谢改变中的观察结果得到转录组学分析的支持。FTIR光谱分析显示,DR5-AS敲低导致脂质/蛋白比升高20.9%,脂质过氧化降低76.6%。此外,我们检测到脂肪脂链长度增加了3.42%,RNA含量较高,糖原含量较低,表明DR5-AS敲除的HeLa细胞代谢活性相对较低。有趣的是,我们在顺铂治疗和DR5-AS敲除HeLa细胞下观察到类似的基因表达模式。结论:这些结果表明DR5-AS lncRNA似乎在HeLa宫颈癌细胞中顺铂介导的大分子和代谢变化中占一部分。
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引用次数: 1
Bone marrow mesenchymal stem cells attenuate LPS-induced acute lung injury in mice by promoting RvE1/ProD1 and modulating Treg/Th17 balance. 骨髓间充质干细胞通过促进RvE1/ProD1和调节Treg/Th17平衡减轻lps诱导的小鼠急性肺损伤。
Pub Date : 2022-01-01 DOI: 10.3906/biy-2107-83
He-Bu Qian, Guijuan Zou, Chao Li, Qi-Fang He, Jun Liu

Acute lung injury (ALI) and its severe form acute respiratory distress syndrome (ARDS) are respiratory failures caused by excessive alveolar inflammation with high mortality. In this study, we investigated the effects of bone marrow mesenchymal stem cells (BMSCs) on lung injury of lipopolysaccharide (LPS)-induced ALI and explored the associated mechanisms. BMSCs were isolated, cultured, identified by staining with CD34 and CD44 surface markers. LPS-induced ALI mouse model was generated by injecting with LPS and divided into ALI group and ALI+BMSCs group. Mice treated without any reagents were assigned as Control, mice transplanted with BMSCs were assigned as BMSCs group. Regulatory T (Treg) and Th17 percentages were evaluated using flow cytometry. Proresolving mediators (resolvin E1 (RvE1), protectin D1 (ProD1)) in lung tissue and cytokines (interleukin-6 (IL-6) and IL-17) in serum were analyzed by ELISA. Myeloperoxidase (MPO) activity was determined. Cultured cells demonstrated typical characteristics of BMSCs. BMSCs transplantation (ALI+BMSCs) obviously alleviated LPS-induced ALI in mice. BMSCs transplantation significantly decreased MPO activity in LPS-induced ALI in mice compared to the Control group (p < 0.05). BMSCs transplantation markedly increased Treg percentages and decreased dendritic cells (DCs) and Th17 cells percentages compared to those of the Control group (p < 0.05). BMSCs transplantation remarkably enhanced RvE1 and ProD1 levels in LPS-induced ALI (ALI+BMSCs) compared to the ALI group (p < 0.05). BMSCs transplantation significantly attenuated IL-6 and IL-17 levels in serum of mice treated with LPS (ALI+BMSCs) compared to those of the ALI group (p < 0.05). In conclusion, BMSCs transplantation effectively attenuated LPS-induced pathological injury of ALI in mice, at least partly through promoting proresolving mediators RvE1 and ProD1 and modulating the balance of Treg/Th17.

急性肺损伤(Acute lung injury, ALI)及其重症急性呼吸窘迫综合征(Acute respiratory distress syndrome, ARDS)是由肺泡过度炎症引起的呼吸衰竭,病死率高。本研究探讨骨髓间充质干细胞(BMSCs)对脂多糖(LPS)诱导的ALI肺损伤的影响,并探讨其相关机制。分离培养骨髓间充质干细胞,用CD34和CD44表面标记物染色鉴定。采用LPS诱导ALI小鼠模型,分为ALI组和ALI+BMSCs组。无任何试剂处理的小鼠为对照组,移植骨髓间充质干细胞的小鼠为骨髓间充质干细胞组。流式细胞术检测调节性T (Treg)和Th17百分比。ELISA法检测肺组织中促分解介质(分解素E1 (RvE1)、保护素D1 (ProD1))和血清中细胞因子(白细胞介素6 (IL-6)、IL-17)。测定髓过氧化物酶(MPO)活性。培养的细胞表现出骨髓间充质干细胞的典型特征。骨髓间充质干细胞移植(ALI+BMSCs)可明显减轻lps诱导的小鼠ALI。与对照组相比,骨髓间充质干细胞移植显著降低lps诱导ALI小鼠的MPO活性(p < 0.05)。与对照组相比,骨髓间充质干细胞移植显著提高Treg百分比,降低树突状细胞(dc)和Th17细胞百分比(p < 0.05)。与ALI组相比,骨髓间充质干细胞移植显著提高了lps诱导的ALI (ALI+骨髓间充质干细胞)中RvE1和ProD1水平(p < 0.05)。与ALI组相比,骨髓间充质干细胞移植能显著降低LPS组(ALI+骨髓间充质干细胞)小鼠血清中IL-6和IL-17水平(p < 0.05)。综上所述,骨髓间充质干细胞移植可有效减轻lps诱导的小鼠ALI病理损伤,至少部分是通过促进RvE1和ProD1的分泌以及调节Treg/Th17的平衡。
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引用次数: 0
Regulatory roles of an atypical ubiquitin ligase UBE2O in orphans of multiprotein complexes for degradation. 非典型泛素连接酶ube20在多蛋白复合物降解孤儿中的调节作用。
Pub Date : 2022-01-01 DOI: 10.3906/biy-2106-63
Yi Lv, Feiyue Xing

UBE2O as an atypical ubiquitin-conjugating enzyme possesses an E2-E3 hybrid enzyme activity. It can regulate substrate levels or transcriptional activities by cooperating with other E3 ubiquitin ligases or forming homomeric complexes displaying intrinsic E2 and E3 activities. UBE2O controls the quality of cell proteome including protein degradation, modification, transport and location. Recent studies reveal that UBE2O plays a vital role in intracellular protein ubiquitination processes by regulating BMP/SMAD, TRAF/NF-κB, mTOR/HIF1a and IL-1β/IRAK4 signaling pathways, c-Maf stability and BAP1 subcellular location, which is proposed as a quality control supervisor of multiprotein complexes for degradation. Its abnormality leads to a variety of physical activity disorders and even occurrence of cancer. UBE2O is entirely distinct in molecular structure and functions from other E2 ubiquitin ligase. Exploring and elucidating regulatory mechanism of UBE2O may identify novel crucial molecular targets so as to pave therapeutic approaches for ubiquitination-associated metabolic disorders and diseases. Here, we particularly feature regulatory pathways of UBE2O in orphans of multiprotein complexes for degradation and its potential application.

UBE2O是一种非典型泛素偶联酶,具有E2-E3杂交酶活性。它可以通过与其他E3泛素连接酶合作或形成具有内在E2和E3活性的同质复合物来调节底物水平或转录活性。UBE2O控制着细胞蛋白质组的质量,包括蛋白质的降解、修饰、运输和定位。最近的研究表明,UBE2O通过调节BMP/SMAD、TRAF/NF-κB、mTOR/HIF1a和IL-1β/IRAK4信号通路、c-Maf稳定性和BAP1亚细胞定位,在细胞内蛋白泛素化过程中起着至关重要的作用,被认为是多蛋白复合物降解的质量控制supervisor。它的异常会导致各种身体活动障碍甚至癌症的发生。ube20在分子结构和功能上与其他E2泛素连接酶完全不同。探索和阐明UBE2O的调控机制可以发现新的关键分子靶点,从而为泛素化相关代谢紊乱和疾病的治疗铺平道路。在这里,我们特别介绍了UBE2O在多蛋白复合物孤儿中降解的调控途径及其潜在的应用。
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引用次数: 0
Melatonin ameliorates cisplatin-induced neurodegeneration in medulla oblongata through the expressions of Aqp-1,-4, inflammation, and apoptosis pathway genes. 褪黑素通过表达Aqp-1、-4、炎症和凋亡通路基因改善顺铂诱导的延髓神经退行性变。
Pub Date : 2022-01-01 DOI: 10.3906/biy-2110-90
Özlem Öztopuz

In this study, the neuroprotective effects of melatonin (MEL) with changes in apoptosis, inflammation, and histopathological morphology were evaluated in the medulla oblongata of cisplatin (CIS) administered rats. Although the side effects of CIS are known in many tissues, its reaction on the medulla oblongata and the molecular association underlying this effect is unclear. Male wistar albino rats were separated into four groups (control, CIS, CIS+MEL, and MEL) (n = 24). CIS and CIS+MEL groups were given 4 mg/kg CIS at 4-day intervals (days 1, 5, 9, and 13) by the first day of the study. The MEL and CIS+MEL groups were given 10 mg/kg MEL daily for 13 days. At the end of the study, the medulla oblongata sections of the rats were harvested on the 14th day, and the changes in gene expressions were examined. Expression levels of inflammation markers (TNF-α and IL-6), apoptotic markers (Bax and Casp-3), and Aqp-1 and Aqp-4 were found to significantly increase with CIS administration. On microscopic examination, hemorrhage, edema, and perivascular edema were detected in the CIS applied group compared with controls. MEL treatment significantly reduced perivascular edema (p = 0.0152) and hemorrhage (p = 0.0087). Besides, there was a significant difference between the control and CIS groups regarding pyknosis and a significant increase in pyknotic neurons in the CIS treatment group (p < 0.001). This study indicates that CIS treatment significantly impaired medulla oblongata, and combined treatment with MEL ameliorates the injury in rats.

本研究对顺铂大鼠延髓中褪黑素(MEL)的神经保护作用与细胞凋亡、炎症和组织病理学形态学的变化进行了评价。虽然CIS在许多组织中的副作用是已知的,但其对延髓的反应以及这种作用背后的分子关联尚不清楚。雄性wistar白化大鼠分为对照组、CIS组、CIS+MEL组和MEL组(n = 24)。在研究的第一天,CIS组和CIS+MEL组每隔4天(第1、5、9和13天)给予4 mg/kg CIS。MEL组和CIS+MEL组每日给予10 mg/kg MEL,连用13 d。研究结束后,于第14天取大鼠延髓切片,检测基因表达变化。炎症标志物(TNF-α和IL-6)、凋亡标志物(Bax和Casp-3)以及Aqp-1和Aqp-4的表达水平随CIS给药显著升高。镜检显示,与对照组相比,CIS应用组出现出血、水肿和血管周围水肿。MEL治疗显著减少了血管周围水肿(p = 0.0152)和出血(p = 0.0087)。此外,对照组与CIS组在固缩方面存在显著差异,CIS组固缩神经元数量显著增加(p < 0.001)。本研究表明,CIS治疗可显著损伤大鼠延髓,且与MEL联合治疗可改善大鼠延髓损伤。
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引用次数: 1
Design and in vitro, in vivo evaluation of antioxidant bioadhesive gels for burn treatment. 抗氧化生物胶粘剂烧伤治疗的设计及体外、体内评价。
Pub Date : 2022-01-01 DOI: 10.55730/1300-0152.2613
Göksel Gökçe, Sinem Yaprak Karavana, Alper Bağriyanik, Çetin Pekçetin, Evren Algin Yapar, Gülşen Aybar Tural, Evren Homan Gökçe

Burn wounds are frequently encountered health problems, which need a new treatment approach especially in terms of good patient compliance. Availability of use of antioxidant agents and bio-adhesive gels in tissue healing can be an alternative as a new approach for wound healing. Antioxidant taurine containing bio-adhesive gels were prepared by using carbopol (CP) 940 and 934. Rheological and texture analyses were carried out on bio-adhesive gels for in vitro characterization. Wound model on Wistar rats was used to evaluate the in vivo evaluation of gels. Rheological and texture analyses showed that a carbopol bioadhesive gel has acceptable topically use dosage characteristics and in combination with Taurine it presented a successful wound healing effect via antioxidant parameters. In conclusion, bio-adhesive CP 940 (2%) gel containing 50 mM taurine could be promising in the treatment of burns by balancing oxidative stress.

烧伤创面是经常遇到的健康问题,需要新的治疗方法,特别是在良好的患者依从性方面。抗氧化剂和生物胶黏剂在组织愈合中的应用可作为伤口愈合的一种新方法。以卡波醇(CP) 940和934为原料制备了含抗氧化牛磺酸的生物胶粘剂凝胶。对生物胶粘剂凝胶进行了流变学和结构分析,以进行体外表征。采用Wistar大鼠伤口模型评价凝胶的体内评价。流变学和结构分析表明,卡波醇生物黏附凝胶具有可接受的外用剂量特性,并与牛磺酸结合使用,通过抗氧化参数显示出成功的伤口愈合效果。结果表明,含50 mM牛磺酸的CP 940(2%)生物胶粘剂可通过平衡氧化应激来治疗烧伤。
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引用次数: 1
Cancer testis antigen PASD1 expression and immunogenicity in human colorectal cancer and polyps. 癌睾丸抗原PASD1在人结直肠癌和息肉中的表达及免疫原性。
Pub Date : 2022-01-01 DOI: 10.55730/1300-0152.2623
Nur Fazilah Sukor, Azyani Yahaya, Ismail Sagap, Rahman Jamal, Nor Adzimah Johdi

Colorectal cancer (CRC) is a malignant tumor arising from a human inner colon lining that may spread to other organs such as the liver and lungs. Per ARNT Sim domain containing 1 (PASD1) is a cancer-testis antigen expressed in cancers including CRC but not in normal tissues except for normal testes. This study aims to study PASD1 protein as a potential target for CRC immunotherapy. A total of 90 CRC and polyps tissue samples were investigated for PASD1 RNA and protein expression using a real-time polymerase chain reaction and immunohistochemical staining, respectively. Matched patients' peripheral blood mononuclear cells were pulsed with PASD1 peptides and measured for immunogenicity, cell cytotoxicity, and cytokine assays. The clinical data were collected and analyzed accordingly. Our results show that PASD1_v2 mRNA expression was highly expressed in CRC (46.0%) and polyps samples (33.3%). Both PASD1-1 and PASD1-2 proteins were expressed in 31.7% of CRC and 29.4% of polyps samples. Protein expression was weak to moderate positive in the cytoplasm and/or nucleus of the tissues. Immune responses towards CD4-specific PASD1 peptides were detected in 21.7% of CRC and 23.5% of polyps patients. The most immunogenic peptide was PASD1 (1) in CRC while PASD1 (3) in polyps. Cytotoxicity effects were detected up to 57.20% observed in CRC samples while IL-17A and IL-6 cytokines were highly expressed. The demographic data suggest that Chinese female patients more than 60 years old, diagnosed with late-stage rectosigmoid tumors may benefit from the PASD1 peptide immunotherapy approach. This is the first report describing CD4-positive T-helper response to the PASD1 positive CRC patients and its cytotoxicity.

结直肠癌(CRC)是一种源自人类结肠内层的恶性肿瘤,可能会扩散到肝脏和肺部等其他器官。Per ARNT Sim domain containing 1 (PASD1)是一种癌睾丸抗原,在包括CRC在内的癌症中表达,但在除正常睾丸外的正常组织中不表达。本研究旨在研究PASD1蛋白作为结直肠癌免疫治疗的潜在靶点。采用实时聚合酶链反应和免疫组织化学染色分别检测90例结直肠癌和息肉组织样本中PASD1 RNA和蛋白的表达。匹配的患者外周血单个核细胞用PASD1肽脉冲,并测量免疫原性、细胞毒性和细胞因子测定。收集临床资料并进行分析。我们的研究结果显示PASD1_v2 mRNA在结直肠癌(46.0%)和息肉(33.3%)中高表达。PASD1-1和PASD1-2蛋白在31.7%的结直肠癌和29.4%的息肉样本中均有表达。在组织的细胞质和/或细胞核中表达弱至中度阳性。在21.7%的结直肠癌患者和23.5%的息肉患者中检测到针对cd4特异性PASD1肽的免疫应答。免疫原性最强的肽是结直肠癌中的PASD1(1),而息肉中的PASD1(3)。白细胞介素- 17a和白细胞介素-6细胞因子高表达时,CRC样品的细胞毒性作用高达57.20%。人口统计数据表明,60岁以上的晚期直肠乙状结肠肿瘤的中国女性患者可能受益于PASD1肽免疫治疗方法。这是第一个描述cd4阳性t辅助反应对PASD1阳性CRC患者及其细胞毒性的报道。
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引用次数: 0
RGS1 serves as an antitumor target to inhibit proliferation of NICN87-DR cells and tumor growth in the gastric cancer mouse model. RGS1作为抗肿瘤靶点,在胃癌小鼠模型中抑制NICN87-DR细胞增殖和肿瘤生长。
Pub Date : 2022-01-01 DOI: 10.55730/1300-0152.2616
Zhixiong Chen, Banglun Liu, Shouru Zhang, Lihui Chen, Yuyu Lv, Hao Sun

Gastric cancer is becoming the 4th leading cause of cancer-associated death worldwide. The purpose of this study was to investigate the role of RGS1 in gastric cancer in vitro and in vivo. Proliferation, migration, invasion, and colony formation of NCIN87 cells and drug-resistant NCIN87 cells (NCIN87-DR) were determined. Cell apoptosis and cell cycle were examined using a flow cytometry assay. RGS1 gene knock-down vector (pLVshshRGS1) and Xenograft tumor mouse model was generated. RGS1 and epithelial-mesenchymal transition (EMT) associated markers, including E-cadherin (E-cad), N-cadherin (N-cad), Slug, and Vimentin were detected using a western blotting assay. Tumor size of Xenograft tumor mouse was measured and Ki67 expression was detected using the immunohistochemical assay. NCIN87-DR cells demonstrated significantly lower proliferation, migration, and invasion compared to those of NCIN87 cells (p < 0.05). NCIN87-DR cells showed obvious early apoptosis and displayed obvious alterations for the cell cycle. NCIN87-DR cells exhibited predominantly higher RGS1 expression than that in NCIN87 cells (p < 0.01). E-cad expression was markedly decreased (p < 0.01) and N-cad (p < 0.05), Slug (p < 0.01), Vimentin (p < 0.05) expressions were significantly increased in NCIN87-DR cells than those in NCIN87 cells. RGS1 gene silence remarkably reduced NCIN87-DR proliferation compared to that in NCIN87-DR cells without treatment (p < 0.01). RGS1 gene-silenced NCIN87-DR cell immunization predominantly inhibited tumor growth in Xenograft tumor mouse than that without RGS1 silence (p < 0.05). RGS1 gene-silenced NCIN87-DR cell immunization significantly downregulated Ki67 expression in tumor tissues compared with that without RGS1 silence. In conclusion, RGS1 gene silence reduced the proliferation of NCIN87-DR cells in vitro and inhibited tumor growth in vivo. Therefore, RGS1 served as an antitumor target for the gastric cancer treatment.

胃癌正在成为全球第四大癌症相关死亡原因。本研究旨在探讨RGS1在体外和体内胃癌中的作用。检测NCIN87细胞和耐药NCIN87细胞(NCIN87- dr)的增殖、迁移、侵袭和集落形成。流式细胞术检测细胞凋亡和细胞周期。构建RGS1基因敲除载体(pLVshshRGS1)和异种移植瘤小鼠模型。采用western blotting法检测RGS1和上皮间质转化(EMT)相关标志物,包括E-cadherin (E-cad)、N-cadherin (N-cad)、Slug和Vimentin。采用免疫组化法检测异种移植瘤小鼠的肿瘤大小和Ki67的表达。与NCIN87细胞相比,NCIN87- dr细胞的增殖、迁移和侵袭能力明显降低(p < 0.05)。NCIN87-DR细胞早期凋亡明显,细胞周期变化明显。NCIN87- dr细胞RGS1表达明显高于NCIN87细胞(p < 0.01)。NCIN87- dr细胞中E-cad表达量显著低于NCIN87细胞(p < 0.01), N-cad (p < 0.05)、Slug (p < 0.01)、Vimentin (p < 0.05)表达量显著高于NCIN87细胞。RGS1基因沉默与未处理NCIN87-DR细胞相比,显著降低了NCIN87-DR细胞的增殖(p < 0.01)。RGS1基因沉默的NCIN87-DR细胞免疫能显著抑制异种移植瘤小鼠的肿瘤生长(p < 0.05)。与RGS1基因沉默的NCIN87-DR细胞免疫相比,RGS1基因沉默的NCIN87-DR细胞免疫可显著下调Ki67在肿瘤组织中的表达。综上所述,RGS1基因沉默在体外抑制NCIN87-DR细胞的增殖,在体内抑制肿瘤生长。因此,RGS1可作为胃癌治疗的抗肿瘤靶点。
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引用次数: 0
Cytoplasmically localized tRNA-derived fragments inhibit translation in Drosophila S2 cells. 胞质定位的trna衍生片段抑制果蝇S2细胞的翻译。
Pub Date : 2022-01-01 DOI: 10.55730/1300-0152.2610
Syed Muhammad Hamid, Bünyamin Akgül
Transfer ribonucleic acids (tRNAs) serve not only as amino acid carriers during translation but also as a template for the biogenesis of short fragments that can regulate gene expression. Despite recent progress in the function of tRNA-derived fragments (tRFs), their intracellular localization, protein partners, and role in regulating translation are not well understood. We used synthetic tRFs to investigate their localization and function in Drosophila S2 cells. Under our experimental setting, all synthetic tRFs tested were localized at distinct sites within the cytoplasm in a similar manner in Drosophila S2 cells. Cytoplasmically-localized tRFs were positioned in close proximity to GW182 and XRN1 proteins. Functionally, tRFs, which slightly suppressed proliferation in S2 cells, inhibited translation without any major shift in the polysome profile. These results suggest that 5′-tRFs are cytoplasmically-localized and regulate gene expression through inhibition of translation in Drosophila.
转移核糖核酸(trna)不仅在翻译过程中充当氨基酸载体,而且作为调控基因表达的短片段生物发生的模板。尽管最近在trna衍生片段(trf)的功能方面取得了进展,但它们在细胞内的定位、蛋白质伴侣以及在调节翻译中的作用尚未得到很好的理解。我们使用合成的tRFs来研究它们在果蝇S2细胞中的定位和功能。在我们的实验环境下,所有被测试的合成tRFs在果蝇S2细胞中以类似的方式定位在细胞质内的不同位置。细胞质定位的tRFs位于GW182和XRN1蛋白附近。在功能上,tRFs虽然能轻微抑制S2细胞的增殖,但却能抑制翻译,而不会导致多体结构发生大的变化。这些结果表明,5′-tRFs在果蝇中存在胞质定位,并通过抑制翻译调节基因表达。
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引用次数: 1
Palmitic acid declines glucose uptake in HepG2 cells via modulating phosphoglucomutase 1 to repress phosphatidylinositol 3 kinase/protein kinase B and JNK pathways via inducing microRNA-124-3p. 棕榈酸通过诱导microRNA-124-3p,通过调节磷酸葡萄糖糖化酶1抑制磷脂酰肌醇3激酶/蛋白激酶B和JNK通路,降低HepG2细胞的葡萄糖摄取。
Pub Date : 2022-01-01 DOI: 10.55730/1300-0152.2618
LingHui Zhang, ShengLi Zhang

Diabetes resulting from insufficient insulin secretion or insulin resistance (IR) is a highly prevalent metabolic disease. Since microRNAs have been linked with elevated IR, the current research hypothesized that miR-124-3p has a role in IR and the establishment of IR and type 2 diabetes (T2DM). The study aimed to explore the molecular mechanisms of miR-124-3p which influence IR leading to T2DM establishment. HepG2 cells were cultured in vitro, and palmitic acid (PA) was used to construct the IR cell model. In the IR model, transfection of miR-124-3p or phosphoglucomutase 1 (PGM1) linked plasmids were transfected into HepG2 cells. RT-qPCR was used to determine the miR-124-3p and PGM1 expressions in the cells. Cell viability was assessed through CCK-8 assays, while glucose consumption was studied using a glucose uptake test. Interaction between miR-124-3p and PGM1 was examined using a dual-luciferase reporter assay. Autophagy, phosphatidylinositol 3 kinases (PI3K)/protein kinase B (AKT) and JNK pathways-linked factors, glucose transporter 4 (GLUT4), and c-Jun were determined through western blotting assays. MiR-124-3p expression was elevated, but PGM1 was reduced in the IR model. Glucose uptake was reduced posttreatment with 0.8 mM PA. There was a significantly increased PI3K, p-PI3K, AKT, p-AKT, GLUT4, LC3I/II, Beclin-1, p-JNK1/2, and c-Jun, but reduced p62 expressions were presented in the PA + miR-124-3p inhibitor compared to the PA and PA + inhibitor NC groups. PGM1 binds directly to miR-124-3p through the 3' UTR region target. Overall, miR-124-3p downregulates glucose consumption via targeting PGM1 to repress PI3K/AKT and JNK pathways. Silencing PGM1 inhibited the suppressor role of miR-124-3p on glucose uptake, cell proliferation, and inflammation. In conclusion, miR-124-3p reduces glucose uptake in HepG2 cells via PGM1/PI3K/AKT modulation. MiR-124-3p targets PGM1 in IR and may provide an effective therapeutic alternative for T2DM.

由胰岛素分泌不足或胰岛素抵抗引起的糖尿病是一种非常普遍的代谢性疾病。由于microrna与IR升高有关,目前的研究假设miR-124-3p在IR以及IR和2型糖尿病(T2DM)的建立中起作用。本研究旨在探讨miR-124-3p影响IR导致T2DM形成的分子机制。体外培养HepG2细胞,用棕榈酸(PA)构建IR细胞模型。在IR模型中,转染miR-124-3p或磷酸葡萄糖糖化酶1 (PGM1)连接质粒转染HepG2细胞。RT-qPCR检测细胞中miR-124-3p和PGM1的表达。通过CCK-8测定细胞活力,通过葡萄糖摄取试验研究葡萄糖消耗。使用双荧光素酶报告基因检测检测miR-124-3p和PGM1之间的相互作用。western blotting检测自噬、磷脂酰肌醇3激酶(PI3K)/蛋白激酶B (AKT)和JNK通路相关因子、葡萄糖转运蛋白4 (GLUT4)和c-Jun。MiR-124-3p在IR模型中表达升高,而PGM1表达降低。0.8 mM PA处理后葡萄糖摄取减少。PI3K、p-PI3K、AKT、p-AKT、GLUT4、LC3I/II、Beclin-1、p-JNK1/2和c-Jun显著升高,但与PA和PA + inhibitor NC组相比,PA + miR-124-3p抑制剂中p62的表达降低。PGM1通过3' UTR区域靶标直接与miR-124-3p结合。总体而言,miR-124-3p通过靶向PGM1抑制PI3K/AKT和JNK通路下调葡萄糖消耗。沉默PGM1可抑制miR-124-3p对葡萄糖摄取、细胞增殖和炎症的抑制作用。综上所述,miR-124-3p通过PGM1/PI3K/AKT调控降低HepG2细胞的葡萄糖摄取。MiR-124-3p在IR中靶向PGM1,可能为T2DM提供有效的治疗选择。
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引用次数: 0
p110α activity at the M-to-G1 transition is critical for cellular proliferation and reentry into the cell cycle. p110α在m - g1过渡期的活性对细胞增殖和重新进入细胞周期至关重要。
Pub Date : 2022-01-01 DOI: 10.55730/1300-0152.2609
Onur Çizmecioğlu

Phosphoinositide 3-kinase (PI3K) signaling pathway is essential for normal physiology and is impaired in diseases such as premalignant hyperproliferative disorders, primary immunodeficiency, metabolic disorders, and cancer. Although the core PI3K pathway components are known today, a long-standing gap in our knowledge of PI3K signaling concerns how distinct PI3K isoforms and their activity patterns contribute to the functional consequences of pathway upregulation. In order to address this issue, we devised a molecular genetic cell model, which allowed temporal regulation of the indispensable PI3K isoform, p110α in distinct stages of the cell cycle. We found that late M and early G1 presence of p110α is key for proper cell cycle progression, whereas its S-phase abundance was redundant. Our results also emphasize a critical dependence of cell cycle reentry on early G1 activity of p110α. Collectively, our findings provide a temporal perspective to p110α activation and offer insight into which wave of PI3K activity could be essential for cell cycle progression.

磷酸肌肽3-激酶(PI3K)信号通路对正常生理至关重要,在恶性前增生性疾病、原发性免疫缺陷、代谢性疾病和癌症等疾病中受损。虽然核心的PI3K通路成分今天是已知的,但我们对PI3K信号传导的认识长期存在空白,即不同的PI3K异构体及其活性模式如何促进通路上调的功能后果。为了解决这个问题,我们设计了一个分子遗传细胞模型,该模型允许在细胞周期的不同阶段对必不可少的PI3K亚型p110α进行时间调控。我们发现M晚期和G1早期p110α的存在是细胞周期正常进展的关键,而其s期丰度是多余的。我们的研究结果还强调了细胞周期再进入对p110α早期G1活性的关键依赖。总的来说,我们的研究结果提供了p110α激活的时间视角,并提供了PI3K活性的哪一波可能对细胞周期进程至关重要的见解。
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引用次数: 1
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Turkish journal of biology = Turk biyoloji dergisi
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